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Notes: Responses of perennial ryegrass (Lolium perenne L.) to nitrogen (N) fertilizer application rates and timings vary widely, because water is often limiting. Yield response to N fertilizer application during autumn, late-winter and spring, and the associated efficiency of use of these inputs, was assessed under conditions of non-limiting soil moisture during two, one-year lysimeter studies in Canterbury, New Zealand. There were significant (P 〈 0·05) increases in seed and herbage yields with increasing N fertilizer application. Seed yields differed with year; greatest yields were 300 g m−2 in 1996 and 450 g m−2 in 1997. Seed head numbers (r2=0·77), seeds head−1 (r2=0·92) and herbage yield (r2=0·92) were the major determinants of seed yield in both years. Irrigation required to maintain the soil between 70% and 90% of field capacity was directly related (r2=0·94 and 0·99 in 1996 and 1997 respectively) to increases in herbage yield.Seed yield, seed quality (thousand seed weight and percentage of seed 〉 1·85 mg), efficiency of water use, efficiency of N fertilizer use and apparent N fertilizer recovery were greatest when N fertilizer was applied at a rate of 50 kg N ha−1, 50 or 100 kg N ha−1 and 150 kg N ha−1 in autumn, late-winter and spring respectively; further increases in spring N fertilizer stimulated vegetative growth, but not seed yield.As a management strategy, applying N fertilizer to match the N requirements of the crop during the reproductive stage of growth will result in high yields of high quality seed while minimizing environmental impact.

Notes: We studied 143 young subjects by skin-prick testing to common allergens and by the measurement of non-specific bronchial responsiveness (NSBR). A logistic regression model showed a prevalence odds ratio (POR) for bronchial hyper-responsiveness (PD20 〈 10 μmol methacholine) in house dust positive subjects of 4.10 (95% CI 1.77–9.51, P 〈 0.001), and in mould positive subjects 5.72 (95% CI 2.06–15.9, P 〈 0.001): the PORs for epithelia (2.05, P = 0.12) and grasses (1.78, P = 0.19) were not significant. If bronchial reactivity was assessed as measurable (PD20 〈 102 μmol methacholine) or not. the POR for house-dust-positive subjects was 4.83 (95% CI 2.23–10.5, P 〈 0.001), for moulds was 10.5 (95% CI 2.33–47.5, P 〈 0.001), for epithelia was 4.79 (95% CI 1.91–12.0, P 〈 0.001), and for grasses was 2.21 (95% CI 1.11–4.4, P = 0.022). The results show the risk of bronchial hyper-responsiveness is greater in subjects sensitive to house dust and mould than in those reactive to grasses, and suggests that the presence or absence of increased NSBR in atopic individuals may depend on the antigens to which they become sensitized.

Notes: The results of testing for linkage between atopy and the chromosome 11 marker D11S97 is shown for all the 723 subjects genotyped by us up to January 1992. Lod score estimations were confounded by the high population prevalence of atopy, maternal inheritance of atopy at the 11q locus, genetic heterogeneity, and excess of atopy in families not ascertained through a single proband. Affected sib-pair analysis shows evidence for linkage which is not dependent on the definition of atopy or model specification. We suggest that presentation of sib-pair data will be suitable for meta-analysis of the different studies of genetic linkage and atopy.

Notes: Background Aspirin-induced asthma (AIA) affects one in 10 individuals with adult-onset asthma. It is not known if aspirin sensitivity is due to immune mechanisms or to interference with biochemical pathways.Objective The study aimed to test for possible involvement of the genes of the Major Histocompatibility Complex (MHC) in AIA.Methods HLA-DPB1 and HLA-DRB1 genotyping was carried out by DNA methods in 59 patients with positive challenge tests for AIA and in 48 normal and 57 asthmatic controlsResults The DPB 1*0301 frequency was increased in AIA patients when compared with normal controls (19.5% vs 5.2%, Odds Ratio = 4.4, 95% Confidence Interval (CI) 1.6–12.1, P= 0.002), and compared with asthmatic controls (4.4%, OR = 5.3, 95%CI= 1.9–14.4, P= 0.0001). The frequency of DPB 1*0401 in AIA subjects was decreased when compared with normal controls (28.8% vs 49.0%, OR = 0.42, 95%CI = 0.24–0.74, P= 0.003) and asthmatic controls (45.6%, OR = 0.48, 95%CI = 0.28–0.83, P= 0.008). The results remained significant when corrected for multiple comparisons. There were no significant HLA-DRB 1 associations with AIA.Conclusion The presence of an HLA association suggests that immune recognition of an unknown antigen may be part of the aetiology of AIA.

Notes: Background Stings from bees and wasps can cause systemic reactions which can be fatal in some individuals. In these venom-sensitive patients, specific IgE to the venom is produced and is considered to participate in the adverse reactions. This immune response requires antigen presentation by human leucocyte antigens (HLA) class II molecules, which includes DR and DP, which are present on antigen presenting cells.Objective To test for associations between HLA class II DRB1 and DPB1 alleles and life- threatening sensitivity to both bee and wasp venoms. To establish further whether any associations are independent of the atopy phenotype.Methods A total of 33 bee- and 44 wasp-venom-sensitive patients was studied. DRB1 genotypes were determined by single stranded oligonucleotide (SSO) probing of PCR products, and DPB1 genotypes by amplified fragment length polymorphism (AFLP) analysis. Total and specific IgE were measured using the Pharmacia Immunocap, FEIA. Patients with specific IgE to the venom antigens only were termed monosensitive and those with additional specific IgE to HDM and/or GP were termed polysensitive.Results Allele frequencies were compared to an unrelated control population. The 33 bee- sensitive patients had a greater prevalence of DRB 1*07 alleles than the control subjects, 26% vs 14%, with an odds ratio (OR) of 2.1 (95%CI, 1.2–3.7, P= 0.015, corrected for multiple comparisons, pc 〉 = ns). This association was confined to the 15 monosensitive bee patients, who had a 43% DRB 1*07 allele frequency when compared with 11% in the 18 polysensitive bee patients, OR 6.1 (95%CI, 1.73–22, P= 0.004, pc= 0.05), and when compared with a control group of non-venom subjects, 43% vs 16%, OR 3.9 (95% CI, 1.72–9.0, P= 0.002, pc= 0.02). The 44 wasp-sensitive patients had an increase in the DRB1*11 allele when compared with the control subjects, 13% vs 6%, with an OR 2.2 (95%CI, 1.0–4.6, P= 0.04, pc= NS), and a decreased prevalence of DRB 1*04 alleles, 10% vs 19%, with an OR 0.33 (95%CI, 0.24–0.99, P= 0.04, pc= NS), but these were not significant when multiple comparisons were taken into account. The DPB1 alleles were not significantly different between the venom sensitive patients and the controls.Conclusion Patients monosensitive to bee venom had a significantly greater prevalence of DRB 1 *07 alleles than the non-venom, control population suggesting that IgE responses in these patients may, in part be controlled by immune response HLA class II genes. These results are also suggestive of wasp-sensitive patients having a higher prevalence of DRB1*11 and a lower prevalence of DRB 1*04 than the control population.

Notes: Abstract. In order to test for human histocompatibility leucocyte antigens (HLA) class II restriction of IgE responses, 431 subjects from 83 families were genotyped at the HLA-DR and HLA-DP loci and serotyped for IgE responses to six major allergens from common aero-allergen sources. A possible excess of HLA-DR 1 was found in subjects who were responsive to FeldI compared with those who were not (Odds Ratio (OR) = 2, P = 0.002), and a possible excess of HLA-DR4 was found in subjects responsive to Alt a I (OR = 1–9, P = 0.006). Increased sharing of HLA-DR/DP haplotypes was seen in sibling pairs responding to both allergens. Der p I, Der p II, Phi p V and Can f I were not associated with any definite excess of HLA-DR alleles. No significant correlations were seen with HLA-DP genotype and reactivity to any of the allergens. The results suggest class II HLA restriction is insufficient to account for individual differences in reactivity to common allergens.

Notes: In 105 subjects taken from a student population and aged between 15 and 30 there was a strong positive association between the presence of the atopic state, defined by skin tests, and a high level of non-specific bronchial responsiveness to methacholine (χ2= 10·5, d.f. = 2, P= 0·01). Regression analysis showed a history of asthma, and the symptom of wheeze, to be predominantly predicted by the degree of bronchial responsiveness (R2= 31%), with only a minor independent contribution from the degree of atopy (R2 a furthur 5%). The genetic or other reasons for the association between bronchial responsiveness and atopy may have importance in understanding the aetiology of allergic asthma.

Notes: Background Polymorphisms within the β subunit of the high-affinity receptor for IgE (FcεR1-β) on chromosome 11q13 have been related to atopy and asthma and the lymphotoxin α (LTα) gene on chromosome 6 is implicated in asthma.Objective To elucidate the association of polymorphisms in the FcεR1-β and LTα genes to IgE responses and asthma in a family-orientated rural population.Methods A total of 461 adult farmers, who participated in an epidemiological follow-up study on respiratory symptoms among farmers on the Swedish island of Gotland, were examined. The traits assessed included serum total IgE, IgE antibody responses to 21 common inhalant allergens and asthma.Results The 237G mutation was only detected in seven persons. Atopy was found to be associated with the RsaI-ex7 AB-genotype (OR = 1.9; P = 0.04). The RsaI-ex7 B allele had a significant influence on IgE responses to pollens and dust mites (OR = 5.5; P = 0.03 and OR = 5.2; P = 0.049, respectively). The influence of this allele was stronger when the association towards single dust mite species (Lepidoglyphus destructor) was estimated (OR = 7.1, P = 0.03) and the association increased even more when the major allergen of L. destructor (rLep d 2) was analysed (OR = 11.2, P = 0.02). These associations were independent of sex, age and smoking, and the estimates of RsaI-in2 independent of RsaI-ex7. RsaI-in2, RsaI-ex7 and LTα genotypes were unassociated with total serum IgE. No significant difference in the distribution of RsaI-in2, RsaI-ex7 and LTα genotypes was found among subjects with atopy or asthma compared to healthy controls.Conclusion This study supports the notion that polymorphisms in the FcεR1-β gene have significant effects on IgE responsiveness. Secondly, dust mites in rural populations influence the expression of genes on chromosome 11q13.